These studies are designed to study (1) the cardiac dynamic alterations occurring during the development and maintenance of various experimental hypertensions in conscious instrumented dogs and (2) to study the changes occurring in left ventricular wall tensile stress, contractility and dimensions during the development and maintenance of left ventricular hypertrophy. Dogs will be instrumented so as to permit instantaneous measurements of the changes in atrial, left ventricular and aortic pressures, left ventricular internal and external diameters and the atrial and ventricular electrograms. The derived variables obtained from semi-continuous monitoring of these conscious instrumented dogs will be used to characterize their left ventricular functional response to forcing functions such as pacing or graded increases in afterload. After a suitable control period each of a group of instrumented animals will be subjected to a particular intervention design to produce either experimental hypertension, left ventricular hypertrophy or both. Hypertension will be induced by either renal artery constriction, cerebral ischemia, or partial nephrectomy and salt loading. Left ventricular hypertrophy will be induced by producing either a chronic aortic constriction, bilateral arteriovenous fistula or complete heart block and experimental renal hypertension. Additionally, chronic asynchronous constriction will be induced by long term continuous ventricular pacing in an attempt to produce regional (septal) hypertrophy in dogs with bundle branch block. Cardiac dynamics will be studied in these dogs before and during chronic pacing. The topography and ultrastructure of all sacrificed dogs will be studied. With the aid of a dedicated small digital computer, the data derived from each animal will be studied in terms designed to evalute the three major factors, which modulate left ventricular function, preload, afterload and changes in myocardial contractility. An effort will be made to evaluate (1) the nature and significance of a "cardiac factor" in the pathogenesis of experimental hypertensions; and (2) the significance of wall tensile stress changes in the development and maintenance of left ventricular hypertrophy. BIBLIOGRAPHIC REFERENCES: Teamey, R.J., Cothran, L.N., and Hawthome, E.W. Left apical accelleration. Fed. Proc. 35:557, 1976.